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Background <p>Colorectal cancer (CRC) involves metabolic reprogramming alongside genetic alteration. ATP-citrate lyase (ACLY), the rate-limiting enzyme of <i>de novo</i> lipogenesis, is a validated target of microRNA-22 (<i>miR-22</i>) in tumor tissue. We asked whether both are dysregulated in the circulation of patients with CRC and whether they carry diagnostic value.</p> Methods and Results <p>Serum ACLY (ELISA) and circulating <i>miR-22</i> (RT-qPCR, normalized to U6) were measured in 32 patients with histopathologically confirmed CRC and 31 healthy controls; metabolic activity was assessed by PET/CT SUVmax. Analyses used SPSS and REST 2009.</p> <p><i>miR-22</i> was downregulated in patients (relative expression 0.175; <i>p &lt;</i> 0.001) and serum ACLY was elevated (<i>p =</i> 0.009). Across the whole cohort the two markers were inversely correlated (<i>ρ =</i> −0.362; <i>p =</i> 0.004), but not within the patient group (<i>ρ =</i> −0.128; <i>p =</i> 0.485) or within controls (<i>ρ =</i> −0.180; <i>p =</i> 0.333), indicating that it reflects their opposite direction of change between groups. Serum ACLY was higher in patients with radiologically active tumor involvement on PET/CT (<i>p =</i> 0.047). The ACLY/<i>miR-22</i> ratio separated patients from controls with an AUC of 0.984 (<i>p &lt;</i> 0.001), exceeding serum ACLY alone (AUC = 0.691).</p> Conclusions <p>In this single-center, proof-of-concept study, circulating <i>miR-22</i> and serum ACLY were dysregulated in opposite directions in colorectal cancer, and their ratio discriminated patients from controls (AUC &gt; 0.98). These estimates were obtained in a single-center discovery cohort without an independent validation set and require external validation before any diagnostic use. The data do not demonstrate a direct regulatory interaction between the two markers in the circulation, and require validation in larger, prospective cohorts.</p>

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Downregulation of circulating miR-22 and elevation of serum ATP-citrate lyase in colorectal cancer: a proof-of-concept study

  • 期刊论文

  • 发表日期：

    2026年8月4日

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  • Nazila Sahraei Danalou,
  • Kursat Dikmen,
  • Ece Konac,
  • Orhan Canbolat,
  • Mustafa Kavutcu

摘要

Background

Colorectal cancer (CRC) involves metabolic reprogramming alongside genetic alteration. ATP-citrate lyase (ACLY), the rate-limiting enzyme of de novo lipogenesis, is a validated target of microRNA-22 (miR-22) in tumor tissue. We asked whether both are dysregulated in the circulation of patients with CRC and whether they carry diagnostic value.

Methods and Results

Serum ACLY (ELISA) and circulating miR-22 (RT-qPCR, normalized to U6) were measured in 32 patients with histopathologically confirmed CRC and 31 healthy controls; metabolic activity was assessed by PET/CT SUVmax. Analyses used SPSS and REST 2009.

miR-22 was downregulated in patients (relative expression 0.175; p < 0.001) and serum ACLY was elevated (p = 0.009). Across the whole cohort the two markers were inversely correlated (ρ = −0.362; p = 0.004), but not within the patient group (ρ = −0.128; p = 0.485) or within controls (ρ = −0.180; p = 0.333), indicating that it reflects their opposite direction of change between groups. Serum ACLY was higher in patients with radiologically active tumor involvement on PET/CT (p = 0.047). The ACLY/miR-22 ratio separated patients from controls with an AUC of 0.984 (p < 0.001), exceeding serum ACLY alone (AUC = 0.691).

Conclusions

In this single-center, proof-of-concept study, circulating miR-22 and serum ACLY were dysregulated in opposite directions in colorectal cancer, and their ratio discriminated patients from controls (AUC > 0.98). These estimates were obtained in a single-center discovery cohort without an independent validation set and require external validation before any diagnostic use. The data do not demonstrate a direct regulatory interaction between the two markers in the circulation, and require validation in larger, prospective cohorts.